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1 Surgery, Indiana University School of Medicine, Indianapolis, Indiana, United States
2 Cellular & Integrative Physiology, Indiana University School of Medicine, Indianapolis, Indiana, United States
3 Surgery, Indiana University School of Medicine, Indianapolis IN 46202-2879, Indiana, United States; Cellular & Integrative Physiology, Indiana University School of Medicine, Indianapolis, Indiana, United States; Indiana Center for Vascular Biology and Medicine, Indianapolis, Indiana, United States
4 Surgery, Indiana University Medical Center, Indianapolis, Indiana, United States; Cellular & Integrative Physiology, Indiana University School of Medicine, Indianapolis, Indiana, United States; Indiana Center for Vascular Biology and Medicine, Indianapolis, Indiana, United States
* To whom correspondence should be addressed. E-mail: junthank{at}iupui.edu.
Available studies indicate that both genetic background and aging influence collateral growth capacity, but it is not known how their combination affects collateral growth. We evaluated collateral growth induced by ileal artery ligation in Fischer 344 (F344), Brown Norway (BN) and the first generation hybrid of F344xBN (F1) rats available for aging research from the National Institute of Aging. Collateral growth was determined by paired diameter measurements in anesthetized rats immediately and 7 days post-ligation. In 3 month-old rats, significant collateral growth occurred only in BN (35±11%, p<0.001). Endothelial cell number in arterial cross-sections was also determined as this precedes shear-mediated luminal expansion. Compared to same animal controls, intimal cell number was increased only in BN (92±21%, p<0.001). The increase in intimal cell number and the degree of collateral luminal expansion in BN was not affected by age from 3 to 24 months. Immunohistochemical studies demonstrated that intimal cell proliferation was much greater in collaterals of BN than F1. The remarkable difference between these three strains of rats used in aging research and the lack of an age-related impairment in the BN are novel observations. These rat strains mimic clinical observations of interindividual variation in collateral growth capacity and the impact of age on arteriogenesis and should be useful models to investigate the molecular mechanisms responsible for such differences.
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  M. R. Distasi, J. Case, M. A. Ziegler, M. C. Dinauer, M. C. Yoder, L. S. Haneline, M. C. Dalsing, S. J. Miller, C. A. Labarrere, M. P. Murphy, et al. Suppressed hindlimb perfusion in Rac2-/- and Nox2-/- mice does not result from impaired collateral growth Am J Physiol Heart Circ Physiol, March 1, 2009; 296(3): H877 - H886. [Abstract] [Full Text] [PDF]
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